Evidence map›Paper›PMID 23754617›Full record

ArticleMolecular and cellular biochemistry2013

siRNA-mediated knockdown of SMC1A expression suppresses the proliferation of glioblastoma cells.

Ying Yang, Zhenxing Zhang, Renzhi Wang, Wenbin Ma, Junji Wei, Guilin Li

Abstract read
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In one paragraph

Article in Molecular and cellular biochemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 1 pooled it
1.0field-weighted citation impact, top 23% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

14 citing papers in PubMed, 1 synthesis or guideline pooled it, 23 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 3 institutions in 1 country.

Ying YangDepartment of Neurosurgery, Peking Union Medical College Hospital, Peking Union Medical College and Chinese Academy of Medical Sciences, Wangfujing, Dongcheng District, Beijing, People's Republic of China.
Zhenxing Zhang
Renzhi Wang
Wenbin Ma
Junji Wei
Guilin Li
Peking Union Medical College Hospital · CNChinese Academy of Medical Sciences & Peking Union Medical College · CNJinzhou Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

SMC1A is a member of cohesin complex which has essential functions in cell cycle progression and DNA repair. Therefore, we choose SMC1A as a target gene therapy of glioblastoma. It is well known that glioblastoma has very low survival rate because of ineffectiveness of conventional treatments. This study was designed to explore the possibilities of small interfering RNA (siRNA)-mediated SMC1A silencing as alternative method of treatment. We found that the lentivirus-mediated RNAi system efficiently decreased the expression level of SMC1A. Inhibiting SMC1A expression efficiently (P < 0.001) resulted in inhibiting the proliferation and colony formation of U251 and U87MG cells. Moreover, we found that SMC1A silencing led to S cell-cycle arresting. Collectively, these results demonstrated the possibility of siRNA-mediated silencing of SMC1A as a therapeutic tool for the treatment of glioblastoma.

Indexed as

Gene Knockdown TechniquesBrain NeoplasmsCell CycleCell Cycle ProteinsCell Line, TumorCell ProliferationChromosomal Proteins, Non-HistoneDown-RegulationGene Expression Regulation, NeoplasticGene SilencingGlioblastomaHumansLentivirusRNA, MessengerRNA, Small InterferingStructural Maintenance of Chromosome Protein 1Cell Cycle ProteinsChromosomal Proteins, Non-HistoneRNA, MessengerRNA, Small InterferingStructural Maintenance of Chromosome Protein 1

Identifiers

PMID23754617
OpenAlexW2087852517

What OpenQuestion holds

Textmetadata
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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.